Mechanism of decreased baroreceptor activity in chronic hypertensive rabbits. Role of endogenous prostanoids.

Xie, Peili; Chapleau, Mark W.; McDowell, T. S.; Hajduczok, G.; Abboud, François M.

doi:10.1172/jci114754

Cited by 47 publications

(42 citation statements)

References 35 publications

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“…12 - 13 The rabbits were anesthetized with ketamine (40 mg/kg i.m., Ketalar, Parke-Davis, Morris Plains, NJ.) and acetylpromazine (1 mg/kg i.m., Acepromazine, Tech America, Elwood, Kan.) and the kidneys were exposed via a midline abdominal incision using sterile technique.…”

Section: Induction Of Hypertensionmentioning

confidence: 99%

“…The sinus region was filled with a physiological saline solution. 13 The solution was equilibrated with a 95% 0^5 % CO 2 gas mixture and warmed to 37°C in a temperature-controlled water jacket before use (Pc>2>200 mm Hg, Pco2=25-40 mm Hg, pH=7.3-7.4). The carotid sinus was periodically refilled with fresh warmed solution.…”

Section: Acute Experimentsmentioning

confidence: 99%

“…The nerve and electrodes were covered with Wacker Sil-Gel and the sinus region was bathed with physiological saline. 13 ' 15 -16 Carotid sinus nerve activity was recorded using a Grass high-impedance probe (model HIP511E, Grass Instrument Co., Quincy, Mass.) and a Grass P511 preamplifier (30 Hz to 3-10 kHz bandwidth), displayed on a Tektronix oscilloscope (model 5113, Tektronix, Beaverton, Ore.) and monitored with a loudspeaker.…”

Section: Carotid Sinus Nerve Recordingsmentioning

confidence: 99%

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Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.

et al. 1991

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The purpose of this study was to examine the ability of baroreceptors of renal hypertensive rabbits to reset rapidly during acute changes in arterial pressure. The carotid sinus (CS) was vascularly isolated and baroreceptor activity was recorded during slow ramp increases in CS pressure in hypertensive (one-kidney, one wrap; 127±3 mm Hg) and normotensive (one-kidney, no wrap; 85 ±3 mm Hg) rabbits anesthetized with chloralose. Control measurements were made after holding pressure for 10-15 minutes at the level of arterial pressure recorded before each experiment Baroreceptor threshold pressure (PtJ was higher in hypertensives (78 ±4 mm Hg) compared with normotensives (55 ±3 mm Hg, p<0.05), and nerve activity was less in hypertensives over a wide range of pressure. CS distensibility (sonomicrometers) was not significantly different in the two groups. After increasing holding pressure from control by 30 and 60 mm Hg for 10-15 minutes, the extent of baroreceptor resetting (A P^/A holding pressure x 100%) in normotensives was 39±6% and 33±2%, respectively, but only 14±5% and 9±3% in hypertensives (p<0.05). After decreasing holding pressure by 30 and 60 mm Hg, resetting was similar in normotensives (32±6% and 28±3%) and hypertensives (34±3% and 30±4%). In hypertensive rabbits, acute (10-15 minutes) exposure of baroreceptors to normotension (71 ± 4 mm Hg) decreased Pa, to 62 ±4 mm Hg and increased nerve activity to levels not significantly different from those of normotensive animals without altering CS distensibility. The results indicate that in chronic renal hypertension: 1) further upward resetting of baroreceptors during acute increases in pressure is suppressed; 2) in contrast, downward resetting during acute decreases in pressure is preserved; 3) baroreceptor activity is restored rapidly after brief exposure of the CS to normal pressure; and 4) changes in CS distensibility do not explain decreased baroreceptor activity in chronic hypertension nor restoration of activity after acute normalization of pressure. Impairment of acute upward resetting and preservation of downward resetting should be beneficial since they would oppose further increases in pressure and facilitate lowering of pressure. (Hypertension 1991;17:72-79) B aroreceptors buffer fluctuations in arterial pressure by causing reflexly mediated reciprocal changes in both heart rate and sympathetic nerve activity. 1 These changes keep the level of arterial pressure at a predetermined operating level or set point. When changes in pressure are sustained for several minutes, however, baroreceptors are reset rapidly and the baroreceptor pressure-activity curve shifts in the direction of pressure change to function at a new set point. 2 -5 This allows baroreceptors to buffer fluctuations of arterial pressure effectively because the new pressure set point remains on the steep portion of the reset pressure-activity curve. However, resetting provides positive feedback in the control of arterial pressure. During acute hypotension, baroreceptor activity increase...

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Section: Induction Of Hypertensionmentioning

confidence: 99%

Section: Acute Experimentsmentioning

confidence: 99%

Section: Carotid Sinus Nerve Recordingsmentioning

confidence: 99%

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Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.

et al. 1991

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“…In hypertensive patients, due to alteration in the sympathetic autoregulation of blood pressure and resetting of arterial baroreceptors, MAP of <80mmHg may cause severe tissue hypoxia. [27][28][29][30] Therefore, in the present study we have chosen the target point MAP between 80-90 mmHg. With this MAP, visibility of surgical field was significantly better.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Hypotension Caused By Dexmedetomidine– Fentanyl Combination with that of Midazolam–Fentanyl Combination in Hypertensive Patients Undergoing Tympanoplasty Surgery under MAC

Lavanya¹,

Raju²

2017

AIMDR

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“…Evidence suggests that impaired formation of prostanoids and loss of their sensitizing influence contribute to decreased baroreceptor sensitivity in atherosclerosis and in chronic hypertension. 8 The contribution of endothelial dysfunction to altered baroreceptor reflex control in other diseases such as diabetes and heart failure remains to be determined.…”

mentioning

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Are arterial pressure and deformation the sole determinants of baroreceptor activity? Importance of humoral and endothelial modulation in normal and disease states.

Chapleau¹

1992

Hypertension

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A rterial baroreceptors located in the carotid si-/ \ nuses and aortic arch play a major role in A. \ -control of circulation and regulation of arterial pressure. Increased arterial pressure triggers increased frequency of baroreceptor discharge, which leads to reflex adjustments that buffer the rise in pressure. It is established that baroreceptors are not activated by increases in arterial pressure directly but instead are activated by the increased vascular stretch or strain that accompanies the rise in pressure. Mechanical deformation of the baroreceptor nerve endings is usually considered the primary or even the sole determinant of the frequency of baroreceptor discharge. Are there other factors besides deformation that are important in activation of baroreceptors?In this issue of Hypertension, Wang et al 1 report that exposure of the vascularly isolated carotid sinus in anesthetized dogs to the hormone aldosterone suppresses activation of baroreceptors without a change in vascular stretch as measured with sonomicrometer crystals. What is the mechanism of aldosterone-induced suppression of baroreceptor activity? Wang et al 1 demonstrate that the inhibitory effect of aldosterone is dependent on the presence of intact endothelium and is blocked by the aldosterone receptor antagonist spironolactone. The simplest scenario is that aldosterone binds to its receptor in endothelial cells and alters the release of a diffusable mediator that acts directly on baroreceptor neurons to modulate their sensitivity. This study is the first to show that aldosterone modulates baroreceptor activity and adds to the growing evidence that humoral and endothelial factors modulate to a significant extent the sensitivity of baroreceptors. Evidence for Humoral/Endothelial Modulationof Baroreceptor Activity Numerous studies dating back as far as the 1950s have demonstrated that various neurohumoral factors act locally in the carotid sinuses and aortic arch to modulate baroreceptor activity. 2 The majority of these studies,

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Mechanism of decreased baroreceptor activity in chronic hypertensive rabbits. Role of endogenous prostanoids.

Cited by 47 publications

References 35 publications

Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.

Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.

Comparison of Hypotension Caused By Dexmedetomidine– Fentanyl Combination with that of Midazolam–Fentanyl Combination in Hypertensive Patients Undergoing Tympanoplasty Surgery under MAC

Are arterial pressure and deformation the sole determinants of baroreceptor activity? Importance of humoral and endothelial modulation in normal and disease states.

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